ライフサイエンスコーパス: IGF-2

1 that exhibit affinity binding to insulin and IGF-2.

2 CRC mouse models that express high levels of IGF-2.

3 IGF-2 receptors in the cellular response to IGF-2.

4 rkers Sca-1, Kit, and CD31 and receptors for IGF-2.

5 endent pathway in concert with either EGF or IGF-2.

6 adult bone marrow HSCs express receptors for IGF-2.

7 SNRPN and partly lost imprinting of H19 and IGF-2.

8 berrant post-translational processing of pro-IGF-2.

9 nly at Arg104, resulting in the secretion of IGF-2-(1-104) and free E-peptide.

10 abundant in normal serum, mature IGF-2, and IGF-2-(1-87), in this expression system, which indicates

11 (25% cell death), neutralizing antibodies to IGF-2 (18% cell death), antibody to the IGF receptor (45

12 t of fetal liver CD3+Ter119- cells with anti-IGF-2 abrogated their HSC supportive activity, suggestin

13 but also signaling events induced by EGF and IGF-2-activated receptors.

14 l tumor burden of animals with two wild type IGF-2 alleles (paternal and maternal) was the same as th

15 es with neutralizing antibodies to IGF-1 and IGF-2, an antibody that blocks the type 1 IGF receptor,

16 fect the serum levels of IGF-1 and IL-6, but IGF-2 and IGFBP-3 were increased by 1.6- and 1.8-fold, r

17 MEDI-573 efficiently neutralized IGF-2 and induced apoptosis, which resulted in significa

18 studies suggest that autocrine production of IGF-2 and overexpression of the IGF-1R are important com

19 IGF-2 and prolactin receptor mRNAs colocalize in the mam

20 lin-like growth factor types 1 and 2 (IGF-1; IGF-2) and insulin-like peptides are all members of the

21 es the synthesis of insulin growth factor-2 (IGF-2) and vascular endothelial growth factor (VEGF) B a

22 poietin (TPO), insulin-like growth factor 2 (IGF-2), and fibroblast growth factor-1 (FGF-1) in serum-

23 sulin-like growth factors 1 and 2 (IGF-1 and IGF-2), and glial cell line-derived neurotrophic factor

24 Insulin-like growth factor (IGF)-1, IGF-2, and angiotensin II (Ang II), as well as their rec

25 prolactin-induced alveologenesis; prolactin, IGF-2, and cyclin D1, all of which are overexpressed in

26 olving insulin-like growth factor-1 (IGF-1), IGF-2, and IGF-1 receptor (IGF-1R) by investigating thei

27 at are most abundant in normal serum, mature IGF-2, and IGF-2-(1-87), in this expression system, whic

28 Levels of IGF-1 IGF-2, and IGFBP-3 all correlated with the CRP level in

29 s between the CRP level and levels of IGF-1, IGF-2, and IGFBP-3 in the RA patients (r = 0.62-0.898, P

30 (IL-6), insulin-like growth factor (IGF)-1, IGF-2, and leukemia inhibitory factor in medulloblastoma

31 ing growth factor alpha, insulin, IGF-1, and IGF-2 are important for regeneration/repair in the mamma

32 ferate in response to prolactin and identify IGF-2 as a downstream target of prolactin signaling that

33 we identified insulin-like growth factor 2 (IGF-2) as a potentially important regulator of hemangiom

34 effects were specific to CRCs overexpressing IGF-2, as MEDI-573 did not affect the growth CRC cell li

35 on may act to maintain or transport IGF-1 or IGF-2, as well as modulate the local autocrine and parac

36 convertase family mediate processing of pro-IGF-2 at Arg104.

37 Insulin-like growth factors (IGF-1 and IGF-2) bind to the IGF-1 receptor (IGF-1R), increasing c

38 At 4 days post-lesion, 125I-IGF-2 binding was dramatically increased within the lesi

39 r component of the observed increase in 125I-IGF-2 binding.

40 Moreover, blockade of IGF-2 by MEDI-573 modulated other signaling pathways, su

41 We have found that pro-IGF-2 can initially form two disulfide isomers that unde

42 Alveologenesis is retarded in IGF-2-deficient MECs.

43 ent than the IGF-2 response, suggesting that IGF-2 did not signal exclusively via the IGF-1 receptor.

44 pressed genes, Ins-2 (encodes insulin-2) and Igf-2 (encodes insulin-like growth factor-2), that lie 9

45 After birth IGF-2 expression is extinguished in most tissues, but th

46 Ectopic IGF-2 expression restores alveologenesis in prolactin re

47 Allele-specific H19 and IGF-2 expression was assessed with reverse transcription

48 8 of 17 informative tumors showed biallelic IGF-2 expression.

49 d the adjacent insulin-like growth factor 2 (IGF-2) gene.

50 Levels of IGF-1, IGF-2, IGF binding proteins (IGFBP) 1-3, and IL-6 were m

51 is required for expression of genes encoding IGF-2, IGF-binding protein (IGFBP)-2 and IGFBP-3.

52 of macrophages and fibroblasts via paracrine IGF-2/IGF-2R activation, resulting in the stroma-derived

53 ese findings suggest that blocking the STAT3/IGF-2/IGF-2R intercellular signalling loop may overcome

54 rone-treated monkeys had SF levels of IGF-1, IGF-2, IGFBP-1, and IGFBP-3 that were intermediate betwe

55 s H19 transgene could not rescue the loss of Igf-2 imprinting in trans in H19 deletion mice, implying

56 n, we have characterized the biosynthesis of IGF-2 in a human embryonic cell line.

57 T3-dependent transcriptional upregulation of IGF-2 in cancer cells and recruitment of macrophages and

58 nt change in IGF-1 levels and an increase in IGF-2 in HKCs correlating with an increase in ATP and NA

59 , we investigated the oncogenic potential of IGF-2 in IGF2-overexpressing CRC models and the efficacy

60 This work establishes the presence of IGF-2 in the nucleus of cells cultured from human fetal

61 lin, insulin-like growth factor (IGF)-1, and IGF-2 induce expression of HIF-1alpha, which is required

62 relevant S1P levels, we found that IGF-1 and IGF-2 induced GFP-S1P receptor internalization and that

63 Prolactin induces IGF-2 mRNA and IGF-2 induces cyclin D1 protein in primary MECs.

64 tested seven insulin family peptides, IGF-1, IGF-2, insulin, and insulin-like peptides 3, 4, 6, and 7

65 ding a potential source for the transport of IGF-2 into the CNS.

66 Thus, IGF-2 is a mediator of prolactin-induced alveologenesis;

67 eir HSC supportive activity, suggesting that IGF-2 is the key molecule produced by these cells that s

68 These results demonstrate that overexpressed IGF-2 is the major tumorigenic driver in a subset of CRC

69 Insulin-like growth factor-2 (IGF-2) is expressed in most embryonic tissues and is req

70 ther proteins, insulin-like growth factor 2 (IGF-2) is specifically expressed in fetal liver CD3+ cel

71 that a subset of CRC cell lines express high IGF-2 levels owing to an increased DNA copy number and h

72 americ receptor tyrosine kinase, whereas the IGF-2/ mannose 6-phosphate receptor is a single transmem

73 ll, raising the possibility that insulin and IGF-2 may bind to these structures in the ILPR in chroma

74 Prolactin induces IGF-2 mRNA and IGF-2 induces cyclin D1 protein in primar

75 S, either prior to, or following the lesion, IGF-2 mRNA expression was observed in the choroid plexus

76 While no IGF-2 mRNA expression was observed within the CNS, eithe

77 t detected in any of the cell lines, whereas IGF-2 mRNA transcripts were detected in all of them.

78 ng the RNase protection assay, low levels of IGF-2 mRNA were also detected in all of the cervical can

79 orphisms (SNPs) selected from IGF-1 (n = 9), IGF-2 (n = 1), IGF binding protein 1 (IGFBP1; n = 3), IG

80 Silencing IGF-2 or STAT3 expression in cancer cells or IGF-2R or C

81 levels of IGF-1 (P < 0.001), 1.7-fold higher IGF-2 (P < 0.006), 5.9-fold higher IGFBP-1 (P < 0.02), a

82 ppears to play a critical role in regulating IGF-2 P3 promoter activity in a cell density/differentia

83 s, full-length insulin-like growth factor-2 (IGF-2) P3 promoter is significantly up-regulated during

84 ward understanding how high molecular weight IGF-2 peptides might contribute to tumor progression, we

85 on begins in the trans- Golgi apparatus, but IGF-2 peptides must reach the trans-Golgi network for ol

86 We did not detect the IGF-2 peptides that are most abundant in normal serum, m

87 as found between expression levels of IGF-1, IGF-2, phosphorylated IGF-1R, or epidermal growth factor

88 Only IGF-1 and IGF-2 potently activated ERK1/2.

89 is capable of supporting HSC expansion, and IGF-2, produced by these cells, is an important growth f

90 cervical carcinoma cells, and that autocrine IGF-2 production in cervical cancer cells may participat

91 Treatment with IGF-1 or IGF-2 promoted translocation of green fluorescent protei

92 human hemangioma explant model, we show that IGF-2 promotes sprouting from intact hemangioma tissue.

93 e IGF-1R activated by its ligands (IGF-1 and IGF-2) protects cells from apoptosis, the role of the IG

94 IGF-2 protein was localized primarily to tumor vessels o

95 M6P/IGF-2-R with high affinity, and the M6P/IGF-2-R is required for CTGF-stimulated proliferation in

96 M6P/IGF-2-R knockout cells have a reduced proliferative resp

97 oliferation were measured in cultures of M6P/IGF-2-R knockout fibroblasts.

98 These observations suggest that the M6P/IGF-2-R may be a new antifibrotic target.

99 CTGF binds to the M6P/IGF-2-R with high affinity, and the M6P/IGF-2-R is requi

100 e/insulin-like growth factor 2 receptor (M6P/IGF-2-R) alone, or with CTGF-related growth factors were

101 unoprecipitated by antibodies to CTGF or M6P/IGF-2-R.

102 The mannose 6-phosphate/IGF-2 receptor has been proposed to be a tumor suppresso

103 In contrast, IGF-2 receptor knockdown markedly reduced IGF-2-stimulat

104 hese data indicate that endogenous IGF-1 and IGF-2 receptors can independently initiate ERK1/2 signal

105 nd point to a potential physiologic role for IGF-2 receptors in the cellular response to IGF-2.

106 sed in 80% of the HCC samples, and IGF-I and IGF-2 receptors were overexpressed in 40% and 100% of th

107 IGF-1 response to a greater extent than the IGF-2 response, suggesting that IGF-2 did not signal exc

108 observed previously, both the IGF-1 and the IGF-2 responses were sensitive to pertussis toxin and th

109 Pretreatment of IGF-1R(+) hCSCs with IGF-2 resulted in the formation of more mature myocytes

110 )-1 receptor signaling pathways by IGF-1 and IGF-2 results in mitogenic and anabolic effects.

111 Neither BDNF, NT-3, NT-4, LIF, IGF-1 or IGF-2 - singly or in combination - caused any significan

112 We recently reported that IGF-1 and IGF-2 stimulate the ERK1/2 cascade by triggering sphingo

113 ogenic activity, but it inhibited IGF-1- and IGF-2-stimulated cell proliferation.

114 t, IGF-2 receptor knockdown markedly reduced IGF-2-stimulated ERK1/2 phosphorylation, with no effect

115 ed, when combined with other growth factors, IGF-2 supports a 2-fold expansion of day-15 fetal liver

116 addition to IGF-1, IGF-1R(+) hCSCs secreted IGF-2 that promoted myocyte differentiation.

117 umors secrete high molecular weight forms of IGF-2 that result from aberrant post-translational proce

118 mbers, insulin-like growth factor-1 (IGF-1), IGF-2, transforming growth factor-alpha (TGF-alpha), and

119 growth, but an antisense oligonucleotide to IGF-2 uniformly inhibited the EGF-induced mitogenic effe

120 IGF-2-, VEGF-B- or VEGF-D-stimulated chondrosarcoma cell

121 nhibitory effect was abolished when IGF-1 or IGF-2 was added in molar excess, suggesting that IGFBP-1

122 IGF-2 was highly expressed during the proliferative phas

123 Although IGF-2 was predictably less potent than IGF-1 in activati

124 cipitation and subsequent analysis by (125)I-IGF-2 Western ligand blotting (WLB), radioimmunoassay, o

125 essing only IGF-1R synthesize both IGF-1 and IGF-2, which are potent modulators of stem cell replicat